Does Notch play a tumor suppressor role across diverse squamous cell carcinomas?

Zhang, Min; Biswas, Sanjib; Xin, Qin; Gong, Wenrong; Deng, Wenbing; Yu, Hongjun

doi:10.1002/cam4.731

Cited by 47 publications

(33 citation statements)

References 97 publications

(151 reference statements)

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“…Ca2+ can promote activation of Notch 1 and p53 [54].The role of Notch pathway in the tumorigenesis is highly variable. It can be tumor suppressive or pro-oncogenic and can either suppress or promote differentiation typically depend on the cellular context [69,72]. The results of our study and others mentioned here, regarding the mechanism of action of EMF on differentiation are summarized in (Fig.9.)…”

Section: Differentiationsupporting

confidence: 61%

Electromagnetic Field and Temozolomide Increase Differentiation of Human Glioblastoma Cell Line; concise view of mechanism

Ahmadi-Zeidabadi

Akbarnejad

Esmaeeli

et al. 2018

Preprint

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Glioblastoma is a highly malignant brain tumor with an extremely dismal prognosis, with a median survival of 12 months. Promoting glioma stem cell (GSC) differentiation is a crucial therapeutic strategy in treating glioblastoma to improve survival. We combine standard chemotherapy drug Temozolomide (TMZ) with Electromagnetic Field to evaluate their differentiation effects on glioma U87 cell line. Human glioma U87 cells exposed to electromagnetic field (EMF), Temozolomide (TMZ) alone and a combination of both were compared to control group. Nestin and CD133 were detected to identify stem-like cells (SLCs) changes during the experiment. The differentiation was found through detecting the expression of the glial fibrillary acidic protein (GFAP), and Notch4. We evaluated Ca + , SOD, and Notch as important chemical mediators in signal transduction to elucidate the mechanism of actions in the processes of differentiation. The expression of cancer SLC markers CD133, and neural stem/progenitor Nestin decreased in EMF/ Drug combined group compared to control which shows depletion of stem-like cell pool. In contrast, the differentiation of SLCs was increased by detecting the expression of the glial fibrillary acidic protein (GFAP), but, Notch4 decreased in Electromagnetic field/Drug combined group compared to control which shows a benign process of treatment. The differentiation was also confirmed by light microscopy. Morphological changes such as an elongated shape with elongated neurites, intercellular connection, and neurite branching were observed. Superoxide dismutase (SOD), Ca + and Notch were also increased as important chemical mediators in signal transduction. Here, we found the combination of pulsed electromagnetic fields (PEMFs) and TMZ significantly resulted in differentiation and glioma stem cells (GSCs) pool reduction that could have a profound therapeutic implication.

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Section: Differentiationsupporting

confidence: 61%

Electromagnetic Field and Temozolomide Increase Differentiation of Human Glioblastoma Cell Line; concise view of mechanism

Ahmadi-Zeidabadi

Akbarnejad

Esmaeeli

et al. 2018

Preprint

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“…Interestingly, Notch signaling pathway was validated to play tumor suppressive functions in several types of human cancers, suggesting that Notch functions depend on the cellular context [ 42 ]. Since Notch-1 could be an effective target to treat nasopharyngeal carcinoma, development of Notch-1 inhibitors is important for the treatment of NPC.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Notch-1 pathway is involved in rottlerin-induced tumor suppressive function in nasopharyngeal carcinoma cells

et al. 2017

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Recent studies have revealed that rottlerin is a natural chemical drug to exert its anti-cancer activity. However, the molecular mechanisms of rottlerin-induced tumor suppressive function have not been fully elucidated. Notch signaling pathway has been characterized to play a crucial role in tumorigenesis. Therefore, regulation of Notch pathway could be beneficial for the treatment of human cancer. The aims of our current study were to explore whether rottlerin could suppress Notch-1 expression, which leads to inhibition of cell proliferation, migration and invasion in nasopharyngeal carcinoma cells. We performed several approaches, such as CTG, Flow cytometry, scratch healing assay, transwell and Western blotting. Our results showed that rottlerin treatment inhibited cell growth, migration and invasion, and triggered apoptosis, and arrested cell cycle to G1 phase. Moreover, the expression of Notch-1 was obvious decreased in nasopharyngeal carcinoma cells after rottlerin treatment. Importantly, overexpression of Notch-1 promoted cell growth and invasion, whereas down-regulation of Notch-1 inhibited cell growth and invasion in nasopharyngeal carcinoma cells. Notably, we found the over-expression of Notch-1 could abrogate the anti-cancer function induced by rottlerin. Strikingly, our study implied that Notch-1 could be a useful target of rottlerin for the prevention and treatment of human nasopharyngeal carcinoma.

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“…Amplification of XXYLT1 is reported in many types of cancers, including lung, esophagus, and head and neck derived SCC, where a tumor-suppressive role of Notch signaling has been suggested (Yu et al, 2015). Particularly in esophageal cancer, the survival time is significantly shorter in patients with this gene amplification than in patients without the amplification (Zhang, Biswas, et al, 2016).…”

Section: Cancermentioning

confidence: 97%

Effects of Notch glycosylation on health and diseases

Urata

Takeuchi

2019

Dev Growth Differ

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Notch signaling is an evolutionarily conserved signaling pathway and is essential for cell-fate specification in metazoans. Dysregulation of Notch signaling results in various human diseases, including cardiovascular defects and cancer. In 2000, Fringe, a known regulator of Notch signaling, was discovered as a Notch-modifying glycosyltransferase. Since then, glycosylation-a post-translational modification involving literal sugars-on the Notch extracellular domain has been noted as a critical mechanism for the regulation of Notch signaling. Additionally, the presence of diverse Oglycans decorating Notch receptors has been revealed in the extracellular domain epidermal growth factor-like (EGF) repeats. Here, we concisely summarize the recent studies in the human diseases associated with aberrant Notch glycosylation. K E Y W O R D S

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Does Notch play a tumor suppressor role across diverse squamous cell carcinomas?

Cited by 47 publications

References 97 publications

Electromagnetic Field and Temozolomide Increase Differentiation of Human Glioblastoma Cell Line; concise view of mechanism

Electromagnetic Field and Temozolomide Increase Differentiation of Human Glioblastoma Cell Line; concise view of mechanism

Inhibition of Notch-1 pathway is involved in rottlerin-induced tumor suppressive function in nasopharyngeal carcinoma cells

Effects of Notch glycosylation on health and diseases

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